Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis

Our plain-English summary of Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis, by J.N. Kline, D.A. Schwartz, M.M. Monick, et al (Chest, 1993).

The study

• Authors: J.N. Kline, D.A. Schwartz, M.M. Monick, C.S. Floerchinger, G.W. Hunninghake
• Journal: Chest
• Published: 1993;104(1):47-53
• Cited by: 65 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

We examined the influence of untreated interstitial lung disease (ILD) on the in vitro release of interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-Ira) from alveolar macrophages (AM); AM were harvested from normal volunteers, ILD patients, and patients with asbestos-related pleural disease but no ILD. AM were cultured for 24 h and assays for IL-1 beta and IL-1ra were done using sensitive and specific enzyme-linked immunosorbent assay. A greater amount of IL-1 beta was detected in AM supernatants from asbestosis, sarcoidosis, and IPF patients than in those from normal subjects. The IL-1 beta:IL-1ra ratio (IL-1 beta activity index [IL-1AI]) was significantly lower in supernatants of normal macrophages compared with macrophage supernatants from individuals with ILD. The IL-1AI correlated with bronchoalveolar lavage cellularity, a marker of disease activity. Current smoking was associated with lower IL-1 beta and IL-1ra release in ILD. The IL-1AI is a convenient method for comparison of IL-1 beta activity between patient populations.

In plain English

This laboratory study measured substances released by alveolar macrophages, immune cells collected by lung washing (bronchoalveolar lavage). Cells came from 10 nonsmoking volunteers and patients with asbestosis (14), asbestos-related pleural disease without interstitial lung disease (16), sarcoidosis (15) or idiopathic pulmonary fibrosis (15). After 24 hours in culture, the authors measured interleukin-1 beta and its blocker, interleukin-1 receptor antagonist. Volunteers' cells released 25 pg/ml of interleukin-1 beta on average. Patient groups released 208 to 257 pg/ml; the authors called only the sarcoidosis (p=0.07) and fibrosis (p=0.08) increases nearly significant. The authors' index (interleukin-1 beta divided by receptor antagonist, times 1,000) averaged 0.73 in volunteers and 63.7 in asbestosis patients (p less than 0.01). In pleural disease it was 5.77, not significantly higher than normal, the authors reported. In interstitial lung disease patients, current smokers' cells released less interleukin-1 beta than nonsmokers' (p less than 0.05); lower receptor antagonist release was not significant (p=0.07). Volunteers were younger than every patient group. Asbestos fiber types and exposure were not described. The authors concluded the index appears useful for comparing patient groups.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) comparison of cytokine release by cultured alveolar macrophages from patient groups and normal volunteers
• Who was studied: 10 normal volunteers who were lifetime nonsmokers, 14 patients with asbestosis, 16 with asbestos-related pleural disease but no interstitial lung disease, 15 with sarcoidosis and 15 with idiopathic pulmonary fibrosis (IPF); all underwent bronchoalveolar lavage
• Exposure: The groups compared were asbestosis and asbestos-related pleural disease, with sarcoidosis and IPF as other lung diseases. The article does not describe fiber types, jobs or doses. Current smoking was also examined.
• Main results:
  • Macrophages from normal volunteers released only small amounts of interleukin-1 beta: 25 plus or minus 10 pg/ml (mean plus or minus SEM)
  • Interleukin-1 beta release by patient groups (mean plus or minus SEM): asbestosis 209 plus or minus 177 pg/ml; asbestos-related pleural disease 208 plus or minus 157 pg/ml; sarcoidosis 257 plus or minus 165 pg/ml; IPF 245 plus or minus 125 pg/ml. The increases in the sarcoidosis (p=0.07) and IPF (p=0.08) groups were described as nearly significant.
  • Normal macrophages released 60 plus or minus 10 ng/ml of interleukin-1 receptor antagonist, significantly more than macrophages from patients with asbestos-related pleural disease (35 plus or minus 9 ng/ml, p less than 0.05)
  • The interleukin-1 beta activity index is released interleukin-1 beta divided by released interleukin-1 receptor antagonist in each subject, multiplied by 1,000. It was 0.73 plus or minus 0.39 in normal volunteers and 63.7 plus or minus 42.81 in asbestosis patients (p less than 0.01 versus normal control subjects).
  • The index was 5.77 plus or minus 3.19 in asbestos-related pleural disease. The authors reported the index was significantly higher than normal in all ILD groups but not in asbestos-related pleural disease.
  • Among ILD patients, macrophages from current smokers released 28 plus or minus 21 pg/ml of interleukin-1 beta and 12 plus or minus 4 ng/ml of receptor antagonist. Macrophages from nonsmoking ILD patients released 300 plus or minus 113 pg/ml of interleukin-1 beta (p less than 0.05) and 30 plus or minus 4 ng/ml of receptor antagonist (p=0.07, not statistically significant).
  • In asbestos-related pleural disease, patients with a high BAL lymphocyte percentage released significantly less interleukin-1 beta than those with a low percentage (275 plus or minus 207 vs 2.5 plus or minus 2.5 pg/ml, p less than 0.05)
  • In each disease, the activity index was higher in the subset the authors considered to have a worse prognosis
  • The normal volunteers were significantly younger than each patient group
• The authors' conclusion: The authors concluded that the interleukin-1 beta activity index appears to be a useful tool for comparing interleukin-1 beta and interleukin-1 receptor antagonist release among patient groups
• Limitations the authors state:
  • The authors noted that cells may behave differently in the alveolus than in laboratory culture
  • Normal volunteers were left out of the smoking analysis because none of them smoked

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Idiopathic, Pulmonary Fibrosis, Interstitial Lung Disease, Asbestos-Related Pleural Disease, Macrophage, Bronchoalveolar Lavage (BAL).

Related studies

• Alveolar macrophage cytokine and growth factor production in a rat model of crocidolite-induced pulmonary inflammation and fibrosis — K.E. Driscoll, J.K. Maurer, et al. (1995)
• Selective differences in macrophage populations and monokine production in resolving pulmonary granuloma and fibrosis — I. Lemaire (1991)
• Bidirectional modulation of TNF-alpha production by alveolar macrophages in asbestos-induced pulmonary fibrosis — S. Ouellet, H. Yang, et al. (1993)
• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts — I. Lemaire, S. Ouellet (1996)
• Chitotriosidase activity in sarcoidosis and some other pulmonary diseases — M. Tercelj, B. Salobir, et al. (2009)
• Contrasting effects of alveolar macrophages and neutrophils on asbestos-induced pulmonary epithelial cell injury — D.W. Kamp, M.M. Dunn, et al. (1994)

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